Life sciences · 1983
The effect of the beta-adrenoreceptor antagonist Ro03-7894 on rat atrial tension development and (-)-[3H]dihydroalprenolol binding to cardiac and lung membranes.
СтатьяПоддержка исследования: вне правительства СШАПоддержка службы здравоохранения СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Baker S P, Posner P
Аннотация
The ability of 1-(5-chloracetylaminobenzfuran-2-yl)-2-isopropylaminoethanol (Ro03-7894) to irreversibly inactivate beta-adrenoreceptors was studied. In isolated rat atria Ro03-7894 (500 microM) depressed and shifted the tension development curve for isoproterenol to the right. After a 2 hour washout period the dose response curve for isoproterenol was further depressed. At a lower dose of Ro03-7894 (50 microM), the isoproterenol dose response curve was also depressed and shifted to the right although after a 2 hour washout, the sensitivity to isoproterenol was restored but the maximum response was still depressed. Ro03-7894 (50 microM) also depressed the tension development response to increasing concentrations of external calcium. The concentration of Ro03-7894 that inhibited (-)-[3H]dihydroalprenolol (DHA) binding by 50% in cardiac and lung membranes was 20 microM. Incubation of rat ventricular or lung membranes for 1 hour with 100 microM Ro03-7894 followed by washing did not change the concentration of beta-adrenoreceptors or the KD values for [3H]DHA binding. Furthermore, neither the concentration of beta-adrenoreceptors nor the KD for [3H]DHA binding was changed in cardiac and lung membranes at 4 or 24 hours after an i.p. injection of 20 mg/kg of Ro03-7894. The results suggested that Ro03-7894 was a relatively weak beta-adrenoreceptor antagonist which under the conditions used did not irreversibly inactivate the receptor but probably depressed tension development in intact atria nonspecifically.